A Twin Study of the Neuropsychological Consequences of Stimulant Abuse

Toomey, Rosemary; Lyons, Michael J.; Eisen, Seth A.; Xian, Hong; Chantarujikapong, Sunanta; Seidman, Larry J.; Faraone, Stephen V.; Tsuang, Ming T.

doi:10.1001/archpsyc.60.3.303

Cited by 76 publications

(51 citation statements)

References 39 publications

(42 reference statements)

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“…(Bouchard, 1998;Winterer and Goldman, 2003) and are often raised together, twins who are discordant for MA abuse provide a valuable quasi-experimental design to control for extraneous confounds. Only one study has investigated the performance of twins who were discordant for MA abuse (Toomey et al, 2003; although Ersche et al, 2012 also compared siblings who were discordant for stimulant dependence on an inhibitory control measure, the vast majority of these participants abused cocaine, not MA). Toomey et al (2003) examined the neuropsychological performance of 50 male twin pairs from the Vietnam Era Twin Registry (31 monozygotic; 19 dizygotic), in which only one of the members had a history of heavy stimulant use.…”

Section: Resultsmentioning

confidence: 99%

An Evaluation of the Evidence that Methamphetamine Abuse Causes Cognitive Decline in Humans

Dean

Groman

Morales

et al. 2012

Neuropsychopharmacol

203

127

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Methamphetamine (MA) is one of the most commonly abused illicit substances worldwide. Among other problems, abuse of the drug has been associated with reduced cognitive function across several domains. However, much of the literature has not attempted to differentiate cognitive difficulties caused by MA abuse from preexisting cognitive difficulties that are likely caused by other factors. Here, we address this question, evaluating evidence for a priori hypotheses pertaining to six lines of research: (a) animal studies; (b) crosssectional human studies; (c) a twin study; (d) studies of changes in cognition with abstinence from MA; (e) studies of changes in brain structure and function with abstinence from MA; and (f) studies of the relationship between the severity of MA abuse and the extent of cognitive deficits observed. Overall the findings were mixed, with some support for a causal relationship between MA abuse and cognitive decline, and other findings suggesting that there is no relationship. The preponderance of the data, however, does support the possibility that MA abuse causes cognitive decline, of unknown duration, in at least some users of the drug. When averaged across individuals, this decline is likely to be mild in early-to-middle adulthood. However, moderator variables are likely to contribute to the presence and/or severity of cognitive decline exhibited by a given individual.

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Section: Resultsmentioning

confidence: 99%

An Evaluation of the Evidence that Methamphetamine Abuse Causes Cognitive Decline in Humans

Dean

Groman

Morales

et al. 2012

Neuropsychopharmacol

203

127

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“…Johnson et al (1998) observed that controlled intravenous administration to eight cocainedependent individuals was associated with improved performance on the Rapid Visual Information Processing Task. Using a co-twin control research design, Toomey et al (2003) observed that in their sample of 50 twin pairs discordant for abuse of cocaine and/or amphetamines , the drug-abusing co-twin displayed significantly better performance on the CPT, though impaired performance on other attentional measures. On the other hand, two more recent investigations (Moeller et al, 2004;Moeller et al, 2005) suggest that cocaine dependence may be associated with attentional impairments.…”

Section: Sustained Attention and Cocaine Usementioning

confidence: 99%

Attentional deficits in cocaine-dependent patients: Converging behavioral and electrophysiological evidence

Gooding

Burroughs

Boutros

2008

Psychiatry Research

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Although there are several reports of patients with cocaine dependence displaying cognitive deficits, the nature of their information processing deficits is not well characterized. In the present study, the attentional performance of cocaine-dependent patients (n = 14) was examined and compared with that of healthy control individuals (n = 15). Attention was assessed using an auditory oddball eventrelated task as well as the Continuous Performance Test (CPT; Identical Pairs version). The cocainedependent group displayed P300 amplitude reduction compared to controls. The group difference in P300 response latency did not reach significance. On the CPT, the cocaine-dependent patients displayed significantly poorer discriminability and greater errors of commission than the controls. There was a positive correlation between performance on the oddball event-related task and performance on the CPT. This investigation provides converging behavioral and electrophysiological evidence of attentional deficits in cocaine-dependent patients.

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“…MA has been shown to produce psychomotor disturbances based on the grooved pegboard test (Volkow et al, 2001d), trailmaking tests (Kalechstein et al, 2003;Simon et al, 2000), finger tapping (Toomey et al, 2003), and reaction time (Richards et al, 1993) tests. It is not clear, however, if these disturbances are secondary effects of subtle parkinsonism or hyperkinetic conditions or if they are independent of extrapyramidal disorders and reflect disturbances in planning, attention, or executive function.…”

Section: Clinical Studiesmentioning

confidence: 99%

“…This conclusion is consistent with the findings by Moszczynska et al (2004) that the neurotoxic effects of prolonged exposure to MA are more pronounced in the cognitive areas of the striatum (ie caudate) than the pure motor areas (ie putamen). Toomey et al (2003) evaluated neuropsychological performance in 50 twin pairs. Subjects were selected for study because one member used stimulants weekly for at least 1 year and the twin sibling never used stimulants.…”

Section: Clinical Studiesmentioning

confidence: 99%

Do Preclinical Findings of Methamphetamine-Induced Motor Abnormalities Translate to an Observable Clinical Phenotype?

Caligiuri

Buitenhuys

2005

Neuropsychopharmacol

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This review summarizes the preclinical literature of the effects of methamphetamine (MA) on subcortical dopaminergic and GABAergic mechanisms underlying motor behavior with the goal of elucidating the clinical presentation of human MA-induced movement disorders. Acute and chronic MA exposure in laboratory animal can lead to a variety of motor dysfunctions including increased locomotor activity, stereotypies, diminished or enhanced response times, and parkinsonian-like features. With the exception of psychomotor impairment and hyperkinesia, MA-induced movement disorders are not well documented in humans. This review attempts to draw parallels between the animal and human changes in basal ganglia neurochemistry associated with MA exposure and offers explanations for why a parkinsonian phenotype is not apparent among individuals who use and abuse MA. Significant differences in the expression of neurotoxicity and presence of multiple environmental and pharmacologic confounds may account for the lack of a parkinsonian phenotype in humans despite evidence of altered dopamine function.

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A Twin Study of the Neuropsychological Consequences of Stimulant Abuse

Abstract: With ideal controls, this study demonstrates that deficits in attention and motor skills persist after 1 year of abstinence from stimulant use and raises hypotheses regarding relative strengths on a vigilance task among abusers.

Cited by 76 publications

References 39 publications

An Evaluation of the Evidence that Methamphetamine Abuse Causes Cognitive Decline in Humans

An Evaluation of the Evidence that Methamphetamine Abuse Causes Cognitive Decline in Humans

Attentional deficits in cocaine-dependent patients: Converging behavioral and electrophysiological evidence

Do Preclinical Findings of Methamphetamine-Induced Motor Abnormalities Translate to an Observable Clinical Phenotype?

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